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Review
. 2010;20(1):1-16.
doi: 10.1615/critreveukargeneexpr.v20.i1.10.

mTOR signaling in cancer cell motility and tumor metastasis

Hongyu Zhou  1 , Shile Huang
Affiliations
Review

mTOR signaling in cancer cell motility and tumor metastasis

Hongyu Zhou et al. Crit Rev Eukaryot Gene Expr. 2010.

Abstract

Tumor cell migration is a key step in the formation of cancer metastasis. The mammalian target of rapamycin (mTOR), a highly conserved and ubiquitously expressed serinethreonine kinase, has been intensely studied for over a decade as a central regulator of cell growth, proliferation, differentiation, and survival. Recent data have shown that mTOR also plays a critical role in the regulation of tumor cell motility and cancer metastasis. Here, we briefly review recent advances regarding mTOR signaling in tumor cell motility. We also discuss recent findings about the mechanism by which rapamycin, a specific inhibitor of mTOR, inhibits cell motility in vitro and metastasis in vivo.

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Figures

Fig. 1
Fig. 1
Schematic structure of mTOR. Various domains discussed in the text are shown.
Fig. 2
Fig. 2
Schematic of IGF-I activation of a signaling pathway to mTOR. mTOR protein exists in two distinct complexes, mTORC1 and mTORC2. mTORC1, which receives input from several upstream pathways, including PI3K/Akt, TSC1/TSC2, and AMPK, phosphorylates downstream effectors S6K and 4EBP1 and regulates ribosome biogenesis, cell growth, autophagy, cell motility and metabolism. mTORC2 phosphorylates Akt at Ser473 and regulates the actin cytoskeleton and cell motility. Arrows represent activation, whereas bars represent inhibition.
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References

    1. Abizaid A, Lansky AJ, Fitzgerald PJ, Tanajura LF, Feres F, Staico R, Mattos L, Abizaid A, Chaves A, Centemero M, Sousa AG, Sousa JE, Zaugg MJ, Schwartz LB. Percutaneous coronary revascularization using a trilayer metal phosphorylcholine-coated zotarolimus-eluting stent. Am J Cardiol. 2007;99:1403–1408. - PubMed
    1. Abraham RT. Mammalian target of rapamycin: immunosuppressive drugs uncover a novel pathway of cytokine receptor signaling. Curr Opin Immunol. 1998;10:330–336. - PubMed
    1. Alessi DR, Kozlowski MT, Weng QP, Morrice N, Avruch J. 3-Phosphoinositide-dependent protein kinase 1 (PDK1) phosphorylates and activates the p70 S6 kinase in vivo and in vitro. Curr Biol. 1998;8:69–81. - PubMed
    1. Alper O, Bergmann-Leitner ES, Bennett TA, Hacker NF, Stromberg K, Stetler-Stevenson WG. Epidermal growth factor receptor signaling and the invasive phenotype of ovarian carcinoma cells. J Natl Cancer Inst. 2001;93:1375–1384. - PubMed
    1. Attoub S, Noe V, Pirola L, Bruyneel E, Chastre E, Mareel M, Wymann MP, Gespach C. Leptin promotes invasiveness of kidney and colonic epithelial cells via phosphoinositide 3-kinase-, rho-, and rac-dependent signaling pathways. FASEB J. 2000;14:2329–2938. - PubMed

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